The microbiota is a set of microorganisms (bacteria, archaea, viruses and eukaryotes) that are specific to each individual. These microorganisms are located on the skin, in the mouth and mainly in the digestive system, which, for 1012 cells per gram and since there are 1.5 to 2 kg of microbiota, counts the presence of millions of different species, i.e., between 3.3 and 8 million according to the experts, and billions for all microorganisms. This microbiota contains more than one hundred fifty times the genes of the host genome.
The microorganisms of the gut microbiota are classified by kingdom (for example, bacteria), phylum (for example, Firmicutes), class (for example, Clostridia), order (for example, Clostridiales), family (for example, Christensenellaceae), genus (for example, Christensenella) and species (for example, Christensenella minuta).
Each individual has his own microbiota, which comes from his history and roots. However, in a cohort, 75% of species are found in 50% of the cohort and 57% in 90% of the cohort. More than 85% of species are shared between Europe, the USA and Japan.
The gut microbiota is not homogenous. For a same individual, it varies in quantity and quality from the stomach (101 with lactobacillus, vellonella, helicobacter) to the duodenum, jejunum, ileum (103 to 107 with bacilli, streptococcaceae, actinobacteria, actinomycinaeae, corynebacteriaeae) and lastly the colon (1012 with lachnospiraceae, bacteriodetes). Certain bacteria (clostridium, lactobacillus, enterococcus) are also found in the mucus that coats the gut wall. The major phyla are relatively stable in an individual, and the differences are found in terms of the species, often by several percentage points of the total microbiota. Thus, pathogenic conditions are difficult to detect, since they come from these specific species.
The anomalies of the host (genetic and environmental) lie in an imbalanced pathogenic flora called pathogenic dysbiosis; the imbalance threshold is difficult to determine, as are the variations in genuses and species, unless there is a biomarker for the anomaly or the disease. For several years, it has been known that the gut microbiota is not only involved in the digestion and transformation of food into energy, but that it also plays a major role in maintaining good health and in the appearance of several diseases. Recent research suggests that the behavior of the brain, the enteroendocrine system or neurovegetative system, or degenerations, are controlled by the microbiota. It is also known that the gut microbiota is a major regulator in immunity and participates heavily in regulating gene expression of the host.
Through dysbiosis, i.e., a change in the composition of the microbiota, the microbiota may be associated with direct pathogenic metabolic disorders such as type 2 diabetes or cardiovascular disease. Furthermore, certain components of the microbiota have been associated with other diseases such as degenerative diseases, gut diseases and certain types of cancer.
The gut microbiota is also directly correlated with the host's weight. Excess weight with comorbidity and obesity, which are defined by a body mass index (BMI) from 25 to 29.9 for overweight and over 30 for obesity, are in fact associated with a pathological dysbiosis of metabolic origin of the gut microbiota.
Excess weight with comorbidities, obesity and metabolic diseases broadly speaking, are devastating our modern societies, in highly developed countries, emerging countries or even developing countries.
The search for reasons for this epidemic has become critical so as not to see a drop in life expectancy in the next 25 years, and particularly to avoid increasing the number of people in poor health and who are dependent in the end-of-life phase.
The key causes for weight gain are imbalanced food intake, in particular saturated fats, fructose and carbohydrates, which may or may not be associated with a highly sedentary lifestyle relative to food intake, i.e., relative to the quantity of energy. However, not everyone responds in the same way to the same food intake. There are in fact in particular differences in terms of the absorption and storage of energy in the form of fats, and these differences are related to the pathological condition of the gut microbiota.
In case of excess weight and obesity, it has been observed that:                the richness and diversity of the microbiota decreases        certain families, genuses and species of pathogens take precedence over others        the pathogenic microbiota has the ability to extract more energy from foods and non-digestible fibers.        
Furthermore, in overweight and obese individuals, a calorie restriction with rebalancing of the diet increases the total richness of the flora by losing body fat mass, but there is a difference in results of the diet depending on the richness of the initial flora. For microbiota that are initially depleted, the results are lower, in particular on the decrease of inflammation and insulin resistance.
Furthermore, the analysis of the microbiota of thin or even anorexic people compared to the obese has established a correlation with certain microorganisms.
A correlation between the phyla and excess weight/obesity has been searched for, and a relationship has been found between the 2 biggest phyla: the relative ratio of Firmicutes to Bacteriodetes increases with the BMI, and the effect on weight loss results in a decrease in the ratio (Damms-machado a 2015, Pekkala s 2015, Remely m 2015, eslinger aj 2014, Bervoets l 2013, Fava f 2013), though this observation has also been invalidated by results demonstrating the opposite (Rahat-Rozenbloom, 2014 Xu P2012, Sefcíková Z 2010).
It is known that the composition of an individual's microbiota is relatively homogenous over time in terms of the phyla (aside from temporary incidents such as antibiotic treatment) but that the genuses may vary, and it is also known that among several individuals, the phyla vary depending on the age, geographical location, ethnicity, lifestyle, etc. It is therefore impossible to establish a standard microbiota for good health, but it is possible to look for the genuses and species that indicate a condition with or without pathology.
Certain enterotypes with the assembly of positive or negative relationships have been determined. In particular, three enterotypes are predominant throughout the world depending on the primacy of the most significant phylum—bacteriodetes, provotella and ruminococcus—but no direct correlation has been able to be established between these enterotypes and metabolic diseases.
For the composition of the microbiota until 2012, it was accepted that the microbiota was built through outside influence and that it was completely acquired from 0 to 3 years through the environment and diet. In a study from November 2014, an international team run by Bruce Ley (Cornell University, NY) published, under the oversight of Julia Goodrich, an article (“Human genetic shape the gut microbiome”, Cell November 6, 159 789-799), which invalidates the single concept of acquisition by introducing the notion of inheritability for several families, genuses and species; she made this observation by studying a British cohort of monozygotic and dizygotic twins and control persons. The strains of the gut microbiota demonstrated as being inheritable are:                families of bacteria in the Firmicutes: lachanospiraceae, ruminococcaceae and christensenellaceae,        an archea in the Methanogens: M. Smithii.         
The family of the Christensenellaceae is the most transmissible family. It in particular comprises the Christensenella genus, and in particular the Christensanella minuta species, which has been defined and cultivated recently by Masami Morotomi in Tokyo, described in the study “Description of christensenella minuta gen. nov.sp.nov. isolated from human faeces, which forms a distinct branch in the other clostridiales, and proposal of christensenellaceae” (M Morotomi 2012 inter. Jour. of systematic and evolution microbiology 62 144-149).
In children, at birth, the richness of Christensenellaceae is 20% in the meconium versus 8.6% for the mother. This proportion next decreases relatively (to be approximately 5%) through the rapid increase of the other phyla, in particular those that will become preponderant, such as Firmicutes, Bacteriodetes, Proteobacteria and Actinobacteria with the introduction of food (for example, animal fat or proteins) and the environment.
The presence of Christensenella is associated with a low BMI as well as a “good health” condition. The higher the relative quantity of Christensenella is, the more the host tends to be lean and healthy. Due to its low relative presence, Christensenella would become the biomarker for pathogenic dysbiosis, a metabolic pathological condition in particular leading to excess weight with comorbidity, obesity and metabolic diseases.
The family of christensenellaceae is the leader of a “consortium” made up of the following families, ranked by decreasing order of importance in metabolic action: dehalobacteriaceae (firmicutes), unclassified clostridiales, tenericutes unclassified geniuses ML615J-28 and RF39, methanobacteriaceae (euryarchaeota), firmicutes unclassified genus SHA-98, peptococcaceae, verrucomicrobiaceae.
The Christensenellaceae family is often positively linked to the abundance of Methagenes, which in turn is correlated to the production of butyrate and propionate, but Christensenellacea does not need this link to express itself in the metabolism, since it contributes directly to the phenotype of the host with which it is associated.
Julia Goodrich (“Human genetic shape the gut microbiome” Cell November 6, 159 789-799) continued her observation in germ-free mice seeded with obese microbiota in 2 groups, only one of which received an implantation of Christensenella, and that presence caused weight gain of less than 30%.
The Christensenellaceae genus is therefore recognized as a marker of leanness, when it is present in sufficient quantities in the gut microbiota. Furthermore, it is a marker of excess weight and obesity when it is present in small quantities in the gut microbiota. The relative increase of Christensenellacea guarantees weight loss, in particular on the fat mass, and is a driving force for metabolic improvement.
Furthermore, these Christensenellacea bacteria would be involved in other metabolic diseases such as diabetes, heart and vascular disease, atherosclerosis, degenerative bone diseases, neurodegenerative diseases, cancers related to the metabolism, autoimmune diseases and metabolic steatosis and steatohepatitis.
Currently, there is a need for a product capable of acting on the gut microbiota to be able to be used to treat the pathogenic microbiota, and consequently to prevent and treat derived metabolic diseases, such as excess weight with comorbidity, obesity, etc.